抄録
Sevoflurane is a widely used volatile anesthetic in clinical practice, but its neural mechanisms of sevoflurane-induced central respiratory depression remain poorly understood. In the present study,we studied the mechanism of sevoflurane-induced central respiratory depression related to GABAA receptors using the isolated brainstem-spinal cord of neonatal rats (0-4 day old). Rhythmic inspiratory burst activity was recorded from the C4 spinal ventral root. The activity of respiratory neurons in the ventrolateral medulla was recorded using a perforated patch-clamp technique. We found that bath-applied sevoflurane decreased C4 inspiratory burst rate and amplitude. C4 burst rate could be reversed by the administration of a GABAA antagonist, bicuculline. Sevoflurane suppressed the firing of action potentials in preinspiratory and expiratory neurons. In contrast, sevoflurane had little effect on firing in inspiratory neurons. Our findings suggest that suppressed action potential of preinspiratory neurons, which is mediated by the GABAA receptor, serves as the neuronal basis of sevoflurane-induced respiratory depression in the newborn rat. [J Physiol Sci. 2007;57 Suppl:S212]
